Conserving indigenous animal genetic resources as a coping strategy to adapt to climate change: the Azikheli Buffalo in Northern Mountains of Pakistan

There are clear signs that the agro-pastoralists in the Himalayan and Hindu-Kush mountain ranges will have less cropping opportunities due to reduced possibilities for irrigated agriculture as a result of climate change. The importance of extensive livestock production based on well adapted livestock species may once again increase. This calls for a better documentation and understanding of the adaptation capabilities of indigenous breeds considering a changing environment. The current study investigates the adaptive traits of the Azikheli buffalo to mountain environments through calculating mean, standard error and percentages for different variables. Results from this study suggest that the brown coat color, the small body size and the high fertility are adaptive traits of the Azikheli buffalo that may well suit harsh mountainous environment conditions with greater climate variability. Local farmers find it hard to sustain the Azikheli buffalo’s key adaptive traits because of a low bull to buffalo ratio, possibility of insemination with semen from imported breeds and a lack of institutional support to conserve the Azikheli breed. The breed is crucial for sustaining custodian communities in these mountains and thus needs to be conserved.

Squirrel Monkeys (Saimiri sciureus) Infected with the Agent of Bovine Spongiform Encephalopathy Develop Tau Pathology

Squirrel monkeys (Saimiri sciureus) were infected experimentally with the agent of classical bovine spongiform encephalopathy (BSE). Two to four years later, six of the monkeys developed alterations in interactive behaviour and cognition and other neurological signs typical of transmissible spongiform encephalopathy (TSE). At necropsy examination, the brains from all of the monkeys showed pathological changes similar to those described in variant Creutzfeldt-Jakob disease (vCJD) of man, except that the squirrel monkey brains contained no PrP-amyloid plaques typical of that disease. Constant neuropathological features included spongiform degeneration, gliosis, deposition of abnormal prion protein (PrP(TSE)) and many deposits of abnormally phosphorylated tau protein (p-Tau) in several areas of the cerebrum and cerebellum. Western blots showed large amounts of proteinase K-resistant prion protein in the central nervous system. The striking absence of PrP plaques (prominent in brains of cynomolgus macaques [Macaca fascicularis] with experimentally-induced BSE and vCJD and in human patients with vCJD) reinforces the conclusion that the host plays a major role in determining the neuropathology of TSEs. Results of this study suggest that p-Tau, found in the brains of all BSE-infected monkeys, might play a role in the pathogenesis of TSEs. Whether p-Tau contributes to development of disease or appears as a secondary change late in the course of illness remains to be determined.